The ADTRP Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited human polyclonal knockout cell population targeting the ADTRP gene. This polyclonal format provides a heterogeneous loss-of-function model for studying ADTRP-dependent signaling in vascular biology and disease. By avoiding single-cell clonal selection, the population-level gene disruption is suitable for diverse functional assays.
HEK293T is a widely used human embryonic kidney epithelial cell line transformed with SV40 large T antigen. This adherent line offers high transgene expression and efficient viral production. Its renal origin and robust growth make it a versatile platform for ectopic expression and signaling studies. In this knockout model, the HEK293T background provides a genetically tractable system to dissect ADTRP molecular functions without tissue-specific interference.
ADTRP encodes an androgen-dependent regulator acting downstream of the androgen receptor (AR). AR, upon activation by androgens like testosterone, transcriptionally regulates ADTRP, which in turn modulates expression of tissue factor pathway inhibitor (TFPI). This signaling controls coagulation and vascular endothelial function. ADTRP interacts with AR and transcriptional co-regulators, influencing lipid metabolism enzymes and endothelial function genes. Dysregulation leads to coronary artery disease through altered lipid metabolism and endothelial dysfunction.
Although HEK293T cells are kidney-derived, their capacity for exogenous and endogenous signaling component expression makes them useful for studying androgen receptor signaling and ADTRP-mediated TFPI regulation. The knockout enables isolated dissection of the androgen?CADTRP?CTFPI axis away from endothelial complexity. Researchers can assess how ADTRP loss affects TFPI and downstream coagulation and lipid modulators. Despite the non-endothelial lineage, this system supports high-throughput interrogation of ADTRP function and interaction networks.
This polyclonal knockout model is ideal for cardiovascular disease research, enabling reconstitution of the androgen?CADTRP?CTFPI pathway to study coronary artery disease and atherosclerosis. It supports endothelial function assays like tube formation and migration after ectopic endothelial regulator expression, and androgen signaling studies via luciferase reporters and TFPI expression analysis. Co-immunoprecipitation maps ADTRP interactions, while TFPI activity and lipid uptake assays link gene disruption to coagulation and metabolism. The population is suitable for drug screening in atherosclerosis and metabolic syndrome. For further details, contact Ascent Research.
